John Kelly - Plant Population Biology and Genetics
Associate Professor
Ph.D., University of Chicago
Phone: (785) 864-3706
Fax: (785) 864-5431
Research Program
* Kin selection.
* Quantitative trait evolution in plant populations.
* Evolution in viruses and other pathogens.
* Molecular evolution.
Statement of Research Interests
It is widely believed that evolutionary processes are too slow to allow direct measurement of genetic changes. For this reason, most applications of evolutionary theory are historical in nature. A theory is tested by comparing its predictions to extant patterns of variation in nature, either within or across taxa. However, when evolutionary changes occur at a rapid pace, it is possible to directly test the dynamical predictions of evolutionary models. There are now many documented examples of rapidly evolving biological systems. One of my primary research interests is to construct and test models that predict observable changes in the genetic composition of such populations. These "dynamical studies" augment historical analyses and directly address a wide range of fundamental questions in evolutionary biology.
My research on rapidly evolving populations has focused on two very different systems: (1) quantitative trait evolution in short-lived plants, and (2) gene sequence evolution in viral pathogens. The plant work falls largely with the field of quantitative genetics. Quantitative genetics provides a natural framework for predicting phenotypic evolution. A major goal of my research program has been to "generalize" quantitative genetic theory to construct models that are realistic for natural plant populations. One focus has been to explore the role of "neighbor interactions". Many plants frequently experience strong fitness-determining interactions with neighboring plants. Because neighboring plants are often genetic relatives, these interactions have a range of novel evolutionary implications. I have explored these implications with both theoretical studies and field experiments on the plant species Impatiens capensis. A second focus of the plant work is on the evolutionary consequences of non-random mating. Many plants have complex mating systems often involving self-fertilization to some degree. Standard quantitative genetic theory assumes random mating and deviations from this assumption affect the relationship between genetic variation and response to selection. I have developed a quantitative genetic model to predict response to selection in a partially selfing population. One notable application of this model is to determine the conditions that self-fertilization is expected to accelerate or retard selection. I am currently testing the empirical adequacy of this model with experimental studies on the species Mimulus guttatus. These studies have recently been expanded to explore the factors that maintain genetic variation in quantitative traits.
The viral work falls within the field of molecular population genetics. Many viral pathogens, including the Human Immunodeficiency Virus (HIV), undergo extensive genetic evolution within a single host. Elucidating the causes and consequences of these genetic changes for disease transmission and pathogenesis is a major challenge for both evolutionary biology and epidemiology. I have developed population genetic methods to detect certain "molecular signatures" of natural selection that may be observed in patterns of viral gene sequence variation. An application of this method to existing sequence data indicate that natural selection has an important effect on genetic variation in HIV populations (within a single infected patient). This selection is likely induced by the immune system of an infected person. The models have also been extended to estimate the average replication rate of HIV in vivo. This analysis can be combined with virological and gene sequence studies to provide novel information about HIV infection, specifically with respect to the role of latently infected cells. This research project is continuing in collaboration with virologists at the KU medical center.
Kelly, J. K. 2005. Epistasis in monkeyflowers. Genetics 171:1917-1931.
Kelly, J. K. 2005. Family-level inbreeding depression and the evolution of plant mating systems. New phytologist 165:55-62.
Kelly, J. K. 2003. Deleterious mutations and the genetic variance of male fitness components in Mimulus guttatus. Genetics 164:1071-1085.
Kelly, J. K, S. Williamson, M. E. Orive, M. Smith, and R. D. Holt. 2003. Linking dynamical and population genetic models of persistent viral infection. American Naturalist 162:14-28.
Kelly, J. K. and J. H. Willis. 2001. Deleterious mutations and genetic variation for flower size in Mimulus guttatus. Evolution 55:937-942.
Kelly, J. K. 1999. Response to selection in partially self fertilizing populations. I. Selection on a single trait. Evolution 53:336-349.
Kelly, J. K. 1997. A test of neutrality based on inter-locus associations. Genetics 146:1197-1206.
Kelly, J. K. 1996. Kin selection in the annual plant Impatiens capensis. American Naturalist 147:899-918.
Kelly, J. K. and M. A. F. Noor. 1996. Speciation by reinforcement: a model derived from studies of Drosophila. Genetics 143:1485-1497.
Kelly, J. K. 1994. An application of population genetic theory to synonymous gene sequence evolution in the human immunodeficiency virus (HIV). Genetical Research 64:1-9.
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